The network of interactions underlying liver regeneration is robust and precise with liver resections resulting in controlled hyperplasia (cell proliferation) that terminates when the liver regains its lost mass. The interplay of cytokines and growth factors responsible for the inception and termination of this hyperplasia is not well understood. We developed a model for this network of interactions based on the known data of liver resections. This model reproduces the relevant published data on liver regeneration and provides geometric insights into the experimental observations. The predictions of this model are used to suggest two novel strategies for speeding up liver mass recovery and a strategy for enabling liver mass recovery in cases where a resection leaves less than 20% of the liver that would otherwise result in complete loss of liver mass. We are collaborating with Dr. Doria, a transplant surgeon at Thomas Jefferson University, to see what changes are required in our model of rat liver regeneration to be able to predict the process in human. The aim is to ascertain which of the numerous parameters in our rat liver model needs to be changed to account for the human process, which appears to take roughly 20 times as long as that in rat. We are systematically varying the parameters in the rat model to find the best human model. Our expectation is that the basic biochemistry remains the same, but that the signaling effects on rates of cellular processes are altered. Work on this is ongoing.